neonatal hypoglyemia aap 2011

7/25/2019 Neonatal Hypoglyemia AAP 2011

1/7

DOI: 10.1542/peds.2010-3851; originally published online February 28, 2011;2011;127;575Pediatrics

Committee on Fetus and NewbornPostnatal Glucose Homeostasis in Late-Preterm and Term Infants

http://pediatrics.aappublications.org/content/127/3/575.full.htmllocated on the World Wide Web at:

The online version of this article, along with updated information and services, is

of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Boulevard, Elk Grove Village, Illinois, 60007. Copyright 2011 by the American Academypublished, and trademarked by the American Academy of Pediatrics, 141 Northwest Point

publication, it has been published continuously since 1948. PEDIATRICS is owned,PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

by guest on August 31, 2013pediatrics.aappublications.orgDownloaded from
http://pediatrics.aappublications.org/content/127/3/575.full.htmlhttp://pediatrics.aappublications.org/content/127/3/575.full.htmlhttp://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/content/127/3/575.full.html


2/7

Clinical ReportPostnatal Glucose Homeostasis in

Late-Preterm and Term Infants

abstractThis report provides a practical guide and algorithm for the screening

and subsequent management of neonatal hypoglycemia. Current evi-

dence does not support a specific concentration of glucose that can

discriminate normal from abnormal or can potentially result in acute

or chronic irreversible neurologic damage. Early identification of the

at-risk infant and institution of prophylactic measures to prevent neo-

natal hypoglycemia are recommended as a pragmatic approach de-

spite the absence of a consistent definition of hypoglycemia in the

literature.Pediatrics2011;127:575579

INTRODUCTION

This clinical report provides a practical guide for the screening and

subsequent management of neonatal hypoglycemia (NH) in at-risk late-

preterm (34 3667weeks gestational age) and term infants. An expert

panel convened by the National Institutes of Health in 2008 concluded

that there has been no substantial evidence-based progress in defining

what constitutes clinically important NH, particularly regarding how it

relates to brain injury, and that monitoring for, preventing, and treat-

ing NH remain largely empirical.1 In addition, the simultaneous occur-

rence of other medical conditions that are associated with brain injury,such as hypoxia-ischemia or infection, could alone, or in concert with

NH, adversely affect the brain.25 For these reasons, this report does

not identify any specific value or range of plasma glucose concentra-

tions that potentially could result in brain injury. Instead, it is a prag-

matic approach to a controversial issue for which evidence is lacking

but guidance is needed.

BACKGROUND

Blood glucose concentrations as low as 30 mg/dL are common in

healthy neonates by 1 to 2 hours after birth; these low concentrations,

seen in all mammalian newborns, usually are transient, asymptomatic,and considered to be part of normal adaptation to postnatal life. 6 8

Most neonates compensate for physiologic hypoglycemia by produc-

ing alternative fuels including ketone bodies, which are released from

fat.

Clinically significant NH reflects an imbalance between supply and use

of glucose and alternative fuels and may result from a multitude of

disturbed regulatory mechanisms. A rational definition of NH must

account for the fact that acute symptoms and long-term neurologic

sequelae occur within a continuum of low plasma glucose values of

varied duration and severity.

David H. Adamkin, MD and COMMITTEE ON FETUS AND

NEWBORN

KEY WORDS

newborn, glucose, neonatal hypoglycemia, late-preterm infant

ABBREVIATIONS

NHneonatal hypoglycemia

D10

Wdextrose 10% in water

This document is copyrighted and is property of the American

Academy of Pediatrics and its Board of Directors. All authors

have filed conflict of interest statements with the American

Academy of Pediatrics. Any conflicts have been resolved through

a process approved by the Board of Directors. The American

Academy of Pediatrics has neither solicited nor accepted any

commercial involvement in the development of the content of

this publication.

The guidance in this report does not indicate an exclusive

course of treatment or serve as a standard of medical care.

Variations, taking into account individual circumstances, may be

appropriate.

www.pediatrics.org/cgi/doi/10.1542/peds.2010-3851

doi:10.1542/peds.2010-3851

All clinical reports from the American Academy of Pediatrics

automatically expire 5 years after publication unless reaffirmed,

revised, or retired at or before that time.

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright 2011 by the American Academy of Pediatrics

FROM THE AMERICAN ACADEMY OF PEDIATRICS

Guidance for the Clinician in

Rendering Pediatric Care

PEDIATRICSVolume 127, Number 3, March 2011 575by guest on August 31, 2013pediatrics.aappublications.orgDownloaded from
http://localhost/var/www/apps/conversion/tmp/scratch_1/pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://localhost/var/www/apps/conversion/tmp/scratch_1/pediatrics.aappublications.org/


3/7

The authors of several literature re-

views have concluded that there is not

a specific plasma glucose concentra-

tion or duration of hypoglycemia that

can predict permanent neurologic in-

jury in high-risk infants.3,9,10 Data that

have linked plasma glucose concentra-tion with adverse long-term neurologic

outcomes are confounded by variable

definitions of hypoglycemia and its du-

ration (seldom reported), the omis-

sion of control groups, the possible in-

clusion of infants with confounding

conditions, and the small number of

asymptomatic infants who were fol-

lowed.3,11,12 In addition, there is no sin-

gle concentration or range of plasma

glucose concentrations that is associ-ated with clinical signs. Therefore,

there is no consensus regarding when

screening should be performed and

which concentration of glucose re-

quires therapeutic intervention in the

asymptomatic infant. The generally

adopted plasma glucose concentra-

tion that defines NH for all infants

(47 mg/dL) is without rigorous sci-

entific justification.1,3,4,9,12

WHICH INFANTS TO SCREEN

Because plasma glucose homeostasis

requires glucogenesis and ketogene-

sis to maintain normal rates of fuel

use,13 NH most commonly occurs in in-

fants with impaired glucogenesis

and/or ketogenesis,14,15 which may oc-

cur with excessive insulin production,

altered counterregulatory hormone

production, an inadequate substrate

supply,1416 or a disorder of fatty acidoxidation.15 NH occurs most commonly

in infants who are small for gesta-

tional age, infants born to mothers

who have diabetes, and late-preterm

infants. It remains controversial

whether otherwise normal infants

who are large for gestational age are

at risk of NH, largely because it is diffi-

cult to exclude maternal diabetes or

maternal hyperglycemia (prediabe-

tes) with standard glucose-tolerance

tests.

A large number of additional maternal

and fetal conditions may also place in-

fants at risk of NH. Clinical signs are

common with these conditions, and it

is likely that patients with such a con-

dition are already being monitored

and that plasma glucose analyses are

being performed.13,17 Therefore, for

practicality, at risk in the manage-

ment approach outlined in Fig 1 in-

cludes only infants who are small for

gestational age, infants who are large

for gestational age, infants who were

born to mothers who have diabetes,

and late-preterm infants. Routine

screening and monitoring of blood glu-

cose concentration is not needed in

healthy term newborn infants after an

entirely normal pregnancy and deliv-

ery. Blood glucose concentration

should only be measured in term in-

fants who have clinical manifestations

orwho are known tobe atrisk. Plasma

or blood glucose concentration should

be measured as soon as possible (min-

utes, not hours) in any infant who man-

ifests clinical signs (see Clinical

Signs) compatible with a low blood

glucose concentration (ie, the symp-

tomatic infant).

Breastfed term infants have lower con-

centrations of plasma glucose but

higher concentrations of ketone bodies

than do formula-fed infants.13,17 It is pos-

tulated that breastfed infants tolerate

lower plasma glucose concentrations

withoutany clinical manifestationsor se-

quelae of NH because of the increased

ketone concentrations.8,1214

WHEN TO SCREEN

Neonatal glucose concentrations de-

crease after birth, to as low as 30

mg/dL during the first 1 to 2 hours af-

ter birth, and then increase to higher

and relatively more stable concentra-

tions, generally above 45 mg/dL by 12

hours after birth.6,7 Data on the optimal

timing and intervals for glucose

screening are limited. It is controver-

sial whether to screen the asymptom-

atic at-risk infant for NH during this

FIGURE 1Screening for and management of postnatal glucose homeostasis in late-preterm (LPT 3436 67

weeks) and term small-for-gestational age (SGA) infants and infants who were born to mothers with

diabetes (IDM)/large-for-gestational age (LGA) infants. LPT and SGA (screen 0 24 hours), IDM and LGA

34 weeks (screen 0 12 hours). IV indicates intravenous.

576 FROM THE AMERICAN ACADEMY OF PEDIATRICSby guest on August 31, 2013pediatrics.aappublications.orgDownloaded from
http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/


4/7

normal physiologic nadir. No studies

have demonstrated harm from a few

hours of asymptomatic hypoglycemia

during this normal postnatal period

of establishing physiologic glucose

homeostasis.9

Infants born to mothers with diabetes

may develop asymptomatic NH as early

as 1 hour after birth18 and usually by 12

hours of age.18 In contrast, infants who

are large for gestational age or small

for gestational age may develop low

plasma glucose concentrations at as

early as 3 hours of age,19 and these

infants may beat riskof NHforup to10

days after birth.20 Therefore, at-risk in-

fants should be screened for NH with a

frequency and duration related to riskfactors specific to the individual in-

fant.5 Screening the asymptomatic at-

risk infant can be performed within

the first hours of birth and continued

through multiple feed-fast cycles. Late-

preterm infants and infants who are

small for gestational age should be fed

every 2 to 3 hours and screened before

each feeding for at least the first 24

hours. After 24 hours, repeated

screening before feedings should becontinued if plasma glucose concen-

trations remain lower than 45 mg/dL.

LABORATORY DATA

When NH is suspected, the plasma or

blood glucose concentration must be

determined immediately by using one

of the laboratory enzymatic methods

(eg, glucose oxidase, hexokinase, or

dehydrogenase method). Plasma

blood glucose values tend to be ap-proximately 10% to 18% higher than

whole-blood values because of the

higher water content of plasma.21,22

Although a laboratory determination is

the most accurate method of measur-

ing the glucose concentration, the re-

sults may not be available quickly

enough for rapid diagnosis of NH,

which thereby delays the initiation of

treatment.23 Bedside reagent test-strip

glucose analyzers can be used if the

test is performed carefully and the cli-

nician is aware of the limited accuracy

of these devices. Rapid measurement

methods available at the bedside in-

clude the handheld reflectance color-

imeter and electrode methods. Theblood sample is usually obtained from

a warmed heel.

Test-strip results demonstrate a rea-

sonable correlation with actual

plasma glucose concentrations, but

the variation from the actual level may

be as much as 10 to 20 mg/dL.2427 Un-

fortunately, this variation is greatest

at lowglucose concentrations. There is

no point-of-care method that is suffi-

ciently reliable and accurate in the lowrange of blood glucose to allow it to be

used as the sole method for screening

for NH.

Because of limitations with rapid

bedside methods, the blood or plasma

glucose concentration must be con-

firmed by laboratory testing ordered

stat. A long delay in processing the

specimen can result in a falsely low

concentration as erythrocytes in the

sample metabolize the glucose in theplasma. This problem can be avoided

by transporting the blood in tubes that

contain a glycolytic inhibitor such as

fluoride.

Screeningof the at-risk infantfor NH and

institution of prophylactic measures to

prevent prolonged or symptomatic NH is

a reasonable goal. Treatment of sus-

pected NH should not be postponed

while waiting for laboratory confirma-

tion. However, there is no evidence toshow that such rapid treatment will mit-

igate neurologic sequelae.

CLINICAL SIGNS

The clinical signs of NH are not specific

and include a wide range of local or

generalized manifestations that are

common in sick neonates.12,13,17 These

signs include jitteriness, cyanosis, sei-

zures, apneic episodes, tachypnea,

weak or high-pitched cry, floppiness or

lethargy, poor feeding, and eye-rolling.

It is important to screen for other pos-

sible underlying disorders (eg, infec-

tion) as well as hypoglycemia. Such

signs usually subside quickly with nor-

malization of glucose supply andplasma concentration.9,13 Coma and

seizures may occur with prolonged NH

(plasma or blood glucose concentra-

tions lower than 10 mg/dL range) and

repetitive hypoglycemia. The more se-

rious signs (eg, seizure activity) usu-

ally occur late in severe and pro-

tracted cases of hypoglycemia and are

not easily or rapidly reversed with glu-

cose replacement and normalization

of plasma glucose concentrations.2830Development of clinical signs may be

ameliorated by the presence of alter-

native substrates.31

Because avoidance and treatment of

cerebral energy deficiency is the prin-

cipal concern, greatest attention

should be paid to neurologic signs. To

attribute signs and symptoms to NH,

Cornblath et al12 have suggested that

the Whipple triad be fulfilled: (1) a low

blood glucose concentration; (2) signsconsistent with NH; and (3) resolution

of signs and symptoms after restoring

blood glucose concentrations to nor-

mal values.12

MANAGEMENT

Anyapproach to management needs to

account for the overall metabolic and

physiologic status of the infant and

should not unnecessarily disrupt the

mother-infant relationship and breast-feeding. The definition of a plasma glu-

cose concentration at which interven-

tion is indicated needs to be tailored to

the clinical situation and the particular

characteristics of a given infant. For

example, further investigation and im-

mediate intravenous glucose treat-

ment might be instituted for an infant

with clinical signs and a plasma glu-

cose concentration of less than 40 mg/




5/7

dL, whereas an at-risk but asymptom-

atic term formula-fed infant may only

require an increased frequency of

feeding and would receive intravenous

glucose only if the glucose values de-

creased to less than 25 mg/dL (birth to

4 hours of age) or 35 mg/dL (424hours of age).32 Follow-up glucose con-

centrations and clinical evaluation

must always be obtained to ensure

that postnatal glucose homeostasis is

achieved and maintained.

Because severe, prolonged, symptom-

atic hypoglycemia may result in neuro-

nal injury,27,28,32 prompt intervention is

necessary for infants who manifest

clinical signs and symptoms. A reason-

able (although arbitrary) cutoff fortreating symptomatic infants is 40 mg/

dL. This value is higher than the physi-

ologic nadir and higher than concen-

trations usually associated with

clinical signs. A plasma sample for a

laboratory glucose determination

needs to be obtained just before giving

an intravenous minibolus of glucose

(200 mgof glucose per kg, 2 mL/kg dex-

trose 10% in water [D10W], intrave-

nously) and/or starting a continuousinfusion of glucose (D

10W at 80100

mL/kg per day). A reasonable goal is to

maintain plasma glucose concentra-

tions in symptomatic infants between

40 and 50 mg/dL.

Figure 1is a guideline for the screen-

ing and management of NH in late-

preterm infants and term infants who

were born to mothers with diabetes,

small for gestational age, or large for

gestational age. In developing a prag-matic approach to the asymptomatic

at-risk infant during the first 24 hours

after birth, mode of feeding, risk fac-

tors, and hours of age were consid-

ered. This strategy is based on the fol-

lowing observations from Cornblath

and Ichord13: (1) almost all infants with

proven symptomatic NH during the

first hours of life have plasma glucose

concentrations lower than 20 to 25

mg/dL; (2) persistent or recurrent NH

syndromes present with equally low

plasma glucose concentrations; and

(3) little or no evidence exists to indi-

cate that asymptomatic NH at any con-

centration of plasma glucose in the

first days of life results in any adversesequelae in growth or neurologic

development.13

Figure 1is divided into 2 time periods

(birth to 4 hours and 4 12 hours) and

accounts for the changing values of

glucose that occur over the first 12

hours after birth. The recommended

values for intervention are intended to

provide a margin of safety over con-

centrations of glucose associated with

clinical signs. The intervention recom-

mendations also provide a range of

values over which the clinician can de-

cide to refeed or provide intravenous

glucose. The target glucose concentra-

tion is greater than 45 mg/dL before

each feeding. At-risk infants should be

fed by 1 hour of age and screened 30

minutes after the feeding. This recom-

mendation is consistent with that of

the World Health Organization. Gavage

feeding may be considered in infantswho are not nippling well. Glucose

screening should continue until 12

hours of age for infants born to moth-

ers with diabetes and those who are

large for gestational age and maintain

plasma glucose concentrations of

greater than 40 mg/dL. Late-preterm

infants and infants who are small for

gestational age require glucose moni-

toring for at least 24 hours after birth,

because they may be more vulnerableto low glucose concentrations, espe-

cially if regular feedings or intrave-

nous fluids are not yet established.20 If

inadequate postnatal glucose ho-

meostasis is documented, the clinician

must be certain that the infant can

maintain normal plasma glucose con-

centrations on a routine diet for a rea-

sonably extended period (through at

least 3 feed-fast periods) before dis-

charge. It is recommended that the at-

risk asymptomatic infant who has glu-

cose concentrations of less than 25

mg/dL (birth to 4 hours of age) or less

than 35 mg/dL (4 24 hours of age) be

refed and that the glucose value be re-

checked 1 hour after refeeding. Subse-quent concentrations lower than 25

mg/dL, or lower than 35 mg/dL,respec-

tively, after attempts to refeed, neces-

sitate treatment with intravenous glu-

cose. Persistent hypoglycemia can be

treated with a minibolus (200 mg/kg [2

mL/kg] D10W) and/or intravenous infu-

sionof D10

W at5 to8 mg/kg per minute,

80 to 100 mL/kg per day; the goal is to

achieve a plasma glucose concentra-

tion of 40 to 50 mg/dL (higher concen-trations will only stimulate further in-

sulin secretion). If it is not possible to

maintain blood glucose concentra-

tions of greater than 45 mg/dL after 24

hours of using this rate of glucose in-

fusion, consideration should be given

to the possibility of hyperinsulinemic

hypoglycemia, which is the most com-

mon cause of severe persistent hypo-

glycemia in the newborn period. A

blood sample should be sent for mea-

surement of insulin along with a glu-

cose concentration at the time when a

bedside blood glucose concentration

is less than 40 mg/dL, and an endocri-

nologist should be consulted.

SUMMARY

Current evidence does not support a

specific concentration of glucose that

can discriminate euglycemia from hy-

poglycemia or can predict that acute

or chronic irreversible neurologic

damage will result. Therefore, similar

to the Canadian Paediatric Society

guidelines, a significantly low concen-

tration of glucose in plasma should be

reliably established and treated to re-

store glucose values to a normal phys-

iologic range.5 Recognizing infants at

risk of disturbances in postnatal glu-

cose homeostasis and providing a

margin of safety by early measures to

578 FROM THE AMERICAN ACADEMY OF PEDIATRICSby guest on August 31, 2013pediatrics.aappublications.orgDownloaded from
http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/


6/7

prevent (feeding) and treat (feeding

and intravenous glucose infusion) low

concentrations are primary goals.

Follow-up glucose measurements are

always indicated to be sure an infant

can maintain normal glucose concen-

trations over several feed-fast cycles.This will also permit recognition of in-

fants with persistent hyperinsulinemic

hypoglycemia and infants with fatty

acid oxidation disorders.

LEAD AUTHOR

David H. Adamkin, MD

COMMITTEE ON FETUS AND NEWBORN,

20092010

Lu-Ann Papile, MD, Chairperson

David H. Adamkin, MD

Jill E. Baley, MD

Vinod K. Bhutani, MD

Waldemar A. Carlo, MD

Praveen Kumar, MD

Richard A. Polin, MD

Rosemarie C. Tan, MD, PhD

Kasper S. Wang, MD

Kristi L. Watterberg, MD

LIAISONS

Capt Wanda Denise Barfield, MD, MPH

Centers for Disease Control and Prevention

William H. Barth Jr, MD American College of

Obstetricians and Gynecologists

Ann L. Jefferies, MD

Rosalie O. Mainous, PhD, RNC, NNP NationalAssociation of Neonatal Nurses

Tonse N. K. Raju, MD, DCH National Institutes

of Health

STAFF

Jim Couto, MA

REFERENCES

1. Hay W Jr, Raju TK, Higgins RD, Kalhan SC,

DevaskarSU. Knowledgegaps and research

needs for understanding and treating neo-

natal hypoglycemia: workshop report from

EuniceKennedyShriverNationalInstitute of

Child Health and Human Development.J Pe-

diatr. 2009;155(5):612 617

2. Adamkin DH. Update on neonatal hypoglyce-

mia.Arch Perinat Med. 2005;11(3):1315

3. Sinclair JC. Approaches to definition of neo-

natal hypoglycemia. Acta Paediatr Jpn.

1997;39(suppl 1):S17S20

4. McGowan JE. Commentary, neonatal hypo-

glycemia. Fifty years later, the questions re-

main the same. Neoreviews. 2004;5(9):

e363e364

5. Canadian Paediatric Society. Screening

guidelines for newborns at risk for low

blood glucose.Paediatr Child Health. 2004;

9(10):723729

6. Srinivasan G, Pildes RS, Cattamanchi G,

Voora S, Lilien LD. Plasma glucose values in

normal neonates: a new look. J Pediatr.

1986;109(1):114117

7. Heck LJ, Erenberg A. Serum glucose levels

in term neonates during the first 48 hours

of life.J Pediatr. 1987;110(1):119122

8. HosethE, JoergensenA, Ebbesen F,MoellerM.

Blood glucose levels in a population of

healthy, breast fed, term infants of appropri-

ate size for gestational age. Arch Dis Child Fe-

tal Neonatal Ed. 2000;83(2):F117F119

9. Rozance PJ, Hay W. Hypoglycemia in newborn

infants:features associated with adverseout-

comes. Biol Neonate. 2006;90(2):74 86

10. Sinclair JC, Steer PA. Neonatal hypoglyce-

mia and subsequent neurodevelopment: a

critique of follow-up studies. Presented at:

CIBA Foundation discussion meeting: Hypo-

glycemia in Infancy; October 17, 1989; Lon-

don, England

11. Boluyt N, van Kempen A, Offringa M. Neuro-

development after neonatal hypoglycemia:

a systematic review and design of an opti-

mal future study. Pediatrics. 2006;117(6):

22312243

12. Cornblath M, Hawdon JM, Williams AF, et al.

Controversies regarding definition of neo-

natal hypoglycemia: suggested operational

th re sh ol ds . Pediatrics. 2000;105(5):

11411145

13. Cornblath M, Ichord R. Hypoglycemia in the

neonate. Semin Perinatol. 2000;24(2):

136149

14. HawdonJM, Ward Platt MP,Aynsley-Green A.

Patterns of metabolic adaptation for pre-

term and term infants in the first neonatal

week. Arch Dis Child. 1992;67(4 spec No.):

357365

15. Kalhan S, Parmimi P. Gluconeogenesis in

the fetus and neonate. Semin Perinatol.2000;24(2):94106

16. Swenne I, Ewald U, Gustafsson J, Sandberg

F, Ostenson C. Inter-relationship between

serum concentrations of glucose, glucagon

and insulin during the first two days of life

in healthy newborns. Acta Paediatr. 1994;

83(9):915919

17. Williams AF. Hypoglycaemia of the newborn:

a review. Bull World Health Organ. 1997;

75(3):261290

18. Agrawal RK, Lui K, Gupta JM. Neonatal hypo-

glycemia in infants of diabetic mothers. J

Paediatr Child Health. 2000;36(4):354 35619. Holtrop PC. The frequency of hypoglycemia

in full-term large and small for gestational

age newborns. Am J Perinatol. 1993;10(2):

150154

20. Hume R, McGeechan A, Burchell A. Failure to

detect preterm infants at risk of hypoglyce-

mia before discharge. J Pediatr. 1999;

134(4):499 502

21. Burrin JM, Alberti KGMM. What is blood

glucose: can it be measured? Diabet Med.

1990;7(3):199206

22. Aynsley-Green A. Glucose: a fuel forthought!

J Paediatr Child Health. 1991;27(1):2130

23. Cornblath M, Schwartz R. Hypoglycemia in

the neonate. J Pediatr Endocrinol. 1993;

6(2):113129

24. Altimier L, Roberts W. One Touch II hospital

system for neonates: correlation with se-

rum glucose values. Neonatal Netw. 1996;

15(2):1518

25. Giep TN, HallRT, HarrisK, Barrick B,Smith S.Eval-

uation of neonatal whole blood versus plasma

glucoseconcentration by ion-selectiveelectrode

technology and comparison with two whole

blood chromogen test strip methods.J Perina-

tol. 1996;16(4):244249

26. Maisels MJ, Lee C. Chemstrip glucose test

strips: correlation with true glucose values

less than 80 mg/dL. Crit Care Med. 1983;

11(4):293295

27. Hussain K, Sharief N. The inaccuracy of ve-

nous and capillary blood glucose measure-

ment using reagent strips in the newborn

period and the effect of haematocrit. Early

Hum Dev. 2000;57(2):111121

28. de Lonlay P, Touati G, Robert JJ, Saudubray

JM. Persistent hyperinsulinaemic hypogly-

caemia.Semin Neonatol. 2002;7(1):95100

29. Meissner T, Brune W, Mayatepek E. Persis-

tent hyperinsulinaemic hypoglycaemia of

infancy: therapy, clinical outcome and mu-

tat ion al ana lys is . Eur J Pediatr. 1997;

156(10):754 757

30. Menni F, deLonlay P, Sevin C, et al. Neuro-

logic outcomes of 90 neonates and infants

with persistent hyperinsulinemic hypogly-

cemia.Pediatrics. 2001;107(3):476479

31. Adam PA, Raiha N, Rahiala EL, Kekomaki M.

Oxidation of glucose and D-B-OH-butyrate by

the early human fetal brain.Acta Paediatr

Scand. 1975;64(1):1724

32. Kalhan S, Peter-Wohl S. Hypoglycemia: what

is it for the neonate? Am J Perinatol. 2000;

17(1):1118




7/7

DOI: 10.1542/peds.2010-3851; originally published online February 28, 2011;2011;127;575Pediatrics

Committee on Fetus and NewbornPostnatal Glucose Homeostasis in Late-Preterm and Term Infants

ServicesUpdated Information &

mlhttp://pediatrics.aappublications.org/content/127/3/575.full.htincluding high resolution figures, can be found at:

References

ml#ref-list-1http://pediatrics.aappublications.org/content/127/3/575.full.htat:This article cites 31 articles, 6 of which can be accessed free

Citations

ml#related-urlshttp://pediatrics.aappublications.org/content/127/3/575.full.htThis article has been cited by 9 HighWire-hosted articles:

Rs)3Peer Reviews (P

Post-Publication

http://pediatrics.aappublications.org/cgi/eletters/127/3/575

Rs have been posted to this article32 P

Subspecialty Collections

_on_fetus__newbornhttp://pediatrics.aappublications.org/cgi/collection/committeeCommittee on Fetus & Newbornthe following collection(s):This article, along with others on similar topics, appears in

Permissions & Licensing

mlhttp://pediatrics.aappublications.org/site/misc/Permissions.xhttables) or in its entirety can be found online at:Information about reproducing this article in parts (figures,

Reprintshttp://pediatrics.aappublications.org/site/misc/reprints.xhtml

Information about ordering reprints can be found online:

rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Grove Village, Illinois, 60007. Copyright 2011 by the American Academy of Pediatrics. Alland trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elkpublication, it has been published continuously since 1948. PEDIATRICS is owned, published,PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

by guest on August 31, 2013pediatrics.aappublications.orgDownloaded from
http://pediatrics.aappublications.org/content/127/3/575.full.htmlhttp://pediatrics.aappublications.org/content/127/3/575.full.htmlhttp://pediatrics.aappublications.org/content/127/3/575.full.htmlhttp://pediatrics.aappublications.org/content/127/3/575.full.html#ref-list-1http://pediatrics.aappublications.org/content/127/3/575.full.html#ref-list-1http://pediatrics.aappublications.org/content/127/3/575.full.html#ref-list-1http://pediatrics.aappublications.org/content/127/3/575.full.html#related-urlshttp://pediatrics.aappublications.org/content/127/3/575.full.html#related-urlshttp://pediatrics.aappublications.org/content/127/3/575.full.html#related-urlshttp://pediatrics.aappublications.org/cgi/collection/committee_on_fetus__newbornhttp://pediatrics.aappublications.org/cgi/collection/committee_on_fetus__newbornhttp://pediatrics.aappublications.org/cgi/collection/committee_on_fetus__newbornhttp://pediatrics.aappublications.org/site/misc/Permissions.xhtmlhttp://pediatrics.aappublications.org/site/misc/Permissions.xhtmlhttp://pediatrics.aappublications.org/site/misc/Permissions.xhtmlhttp://pediatrics.aappublications.org/site/misc/reprints.xhtmlhttp://pediatrics.aappublications.org/site/misc/reprints.xhtmlhttp://pediatrics.aappublications.org/site/misc/reprints.xhtmlhttp://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/http://pediatrics.aappublications.org/site/misc/reprints.xhtmlhttp://pediatrics.aappublications.org/site/misc/Permissions.xhtmlhttp://pediatrics.aappublications.org/cgi/collection/committee_on_fetus__newbornhttp://pediatrics.aappublications.org/content/127/3/575.full.html#related-urlshttp://pediatrics.aappublications.org/content/127/3/575.full.html#ref-list-1http://pediatrics.aappublications.org/content/127/3/575.full.html

neonatal hypoglyemia aap 2011

Documents